title: Exercise training restores decreased cellular immune functions in obese Zucker rats.
abstract: This study investigated whether exercise training had a beneficial effect on the decreased mitogen response and improved a decreased expression of glucose transporter 1 (GLUT-1) in splenocytes from obese Zucker rats. Experimental groups were lean and sedentary and exercise-trained obese Zucker rats. Exercise training, running on a motor-driven treadmill for 5 days/wk for 40 wk, did not induce a significant decrease in body weight in obese Zucker rats. The plasma insulin concentration, showing a significant increase compared with lean Zucker rats, was unaffected by exercise training. However, the plasma triglyceride concentration in obese Zucker rats was significantly depressed by exercise training, whereas it was still higher than that in lean Zucker rats. In addition, natural killer cell activity and concanavalin A-induced mitogenesis of splenic lymphocytes of obese Zucker rats were significantly restored. In these splenic lymphocytes, glucose uptake was significantly lower compared with that in lean Zucker rats, which was also improved by exercise training. Although the expression of GLUT-1, the major glucose transporter in immune cells, was depressed in splenic lymphocytes of obese Zucker rats, exercise training induced a significant improvement. These results suggest that exercise training has a beneficial effect on the decreased cellular immune functions in obese Zucker rats, which is associated, in part, with the improvement in GLUT-1 expression.
authors.affiliation: Department of Nutrition, School of Medicine, The University of Tokushima, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Moriguchi
authors.forename: M
authors.initials: M
authors.lastname: Kato
authors.forename: K
authors.initials: K
authors.lastname: Sakai
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
authors.forename: E
authors.initials: E
authors.lastname: Shimizu
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D006614:Hindlimb / Q000502:physiology; D007111:Immunity, Cellular / Q000276:immunology* / Q000502:physiology*; D007328:Insulin / Q000097:blood; D007694:Killer Cells, Natural / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects; D008934:Mitogens / Q000494:pharmacology; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009124:Muscle Proteins; D009765:Obesity / Q000276:immunology* / Q000503:physiopathology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D011924:Rats, Zucker; D013154:Spleen / Q000166:cytology / Q000187:drug effects; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D007328:Insulin; D008934:Mitogens; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495679:Slc2a1 protein, rat; C495694:Slc2a4 protein, rat; D014280:Triglycerides; D005947:Glucose